Viruses, and viral diseases associated with them, have a common method of propagation. The virus itself infects a few cells in the body. Once in the cell, the viral nucleic acid, DNA or RNA, take over the cell's apparatus, making many copies of itself. An infected cell, or a significant number of infected cells, do not in and of themselves render a mammalian patient ill, even a human. Rather, it is the subsequent release of the virus from the surface of the infected cells that result in wide scale distribution of the virus throughout the body that leads to what regard as illness. It is the marshalling of the body's cellular and chemical defenses to combat this infestation of millions of viral copies that we recognize as the symptoms of viral infection, including fever, weakness, soreness and aches and pains, diarrhea and dehydration, etc. Viral infection, and in particular the symptoms identified can often lead to parasitic or opportunistic infection by secondary agents, including other weaker viruses, bacteria and the like.
Few remedies or treatments are available to combat viral disease. Antibiotics and the like are not only ineffective against viral disease, they may well exacerbate it, by inhibiting defense mechanisms that the body may otherwise bring to bear. In general, upon identification of a set of symptoms as reflecting a disease due to viral infection, or identification of the infectious virus itself, treatment relies on supporting the body's immune systems to deal with the invader. Palliatives including antipyretics and pain relievers, hydration and rest are key support measures. The body is on its own, and in the face of many viruses including a large number of retroviruses, it may not be adequate to face the challenge.
In some few cases, a vaccine or therapeutic focusing on the virus itself may be prepared. Since the 1950s, strategies have focused on preparing “killed” or inactivated forms of the virus, to induce circulating viruses in the host body, or on antisera (antibodies) effective in binding the viral invader. Neither strategy has been has been entirely effective. This due in large measure to the ability of viruses to mutate, and thereby escape the neutralizing effect of the active agent, which is a binding agent, typically an antibody, generated by administration of the passive form (active immunization due to administration of a innocuous or inactive pathogen that induces an immune response that is also effective against the live pathogen) or by administration of an effective titer of antibodies raised against the virus target. Viruses, by shedding or adding epitopes and changing the sequence of their nuclear proteins can in particular, where present, coat proteins, avoid previously effective viruses.
It has been discovered that viruses propagate out of initial infected cells by a process generally referred to as budding. In this process, the virus first invades the cell, and then generates multiple copies of itself within the invaded cell. The invaded cell will ultimately be removed by the bodies own processes. So long as the viral copies do not leave the cells, they cannot replicate the infective process in other cells, and thus do not generate the symptoms or conditions associated with the disease resulting from that viral infection. In the same fashion that a latent virus can reside within a few cells for long periods of time during which the patient is to all intents and appearances healthy, an initial viral infection trapped within a few cells does not pose a health risk, or even inconvenience to the mammalian animal so infected. It is when the virus copies escape from the cell, a process known as budding, that real disease begins.
Budding is effected by “hijacking” a series of proteins and protein complexes, called escort proteins, that carry the virus to the cell membrane, and help create pockets through which the virus escapes the cell. The escort proteins are residents of the cell's cytoplasm, and in normal health process, help a variety of cell synthetic products destined for intra-and-intercellular transmission cross the cell membrane. These escort proteins are not typically present outside the cell, and are ephemerally present, and uniquely accessible, as the time of viral budding. FACS analysis shows concentrations of these proteins on the cell surface at periods associated with viral budding.
An improved therapeutic system for combating viral disease is a goal sought by many. Given the incredible differentiation between viruses, and the mutational abilities of these viruses, no single strategy or agent targeted at the virus is likely to be broadly effective, even within a given virus family, let alone across those families. Even if one does not count the cost in terms of human and commercial animal deaths due to viral infection, the incredible loss of productivity and commercial product, and the billions of dollars of cost in health care and support devoted to viral care annually, make it clear that an improved strategy for treatment of viral infection is required.